Respiratory II (OSA; Asthma; Resp support) Flashcards

1
Q
A
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2
Q

What is the difference between apnoea and hypopnoea? [2]

A

Apnoea – a complete cessation of airflow for
at least 10 seconds

Hypopnoea – a reduction in airflow to under
50% or by 30% for at least 10 seconds with a desaturation of at least 4%

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3
Q

What is Apnoea and Hypopnoea Index? [1]

What are normal, mild, moderate and severe scores? [4]

A

AHI – number of apnoeas and hypopnoeas
per hour of the study

  • 0 to 5 Within normal limits
  • 5 to 15 Mild OSA
  • 15 to 30 Moderate OSA
  • 30 plus Severe OSA
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4
Q

What is the name for the sleep score used for measuring sleep apnoea?

What score is abnormal?
What is the total score

A

Epworth sleepiness scale
10 / 24 is abnormal

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5
Q

What is this? [1]

When is it indicated? [1]

A

Mandibular splint
If CPAP not tolerated

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6
Q

What severity of sleep apnoea is CPAP indicated in? [2]

A

Continuous Positive Airway Pressure (CPAP):
Causes continous air passage to be open
Used for patients with moderate or severe sleep apnoea

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7
Q

Name three conditions that cause macroglossia and therefore sleep apnoea [3]

A

acromegaly, hypothyroidism, amyloidosis

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8
Q

What is the most common surgery for sleep apnoea? [1]

A

Surgery is an option but involves significant surgical reconstruction of the soft palate and jaw. The most common procedure is called uvulopalatopharyngoplasty (UPPP).

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9
Q

A 61-year-old male snores at night, and his wife reports it is so loud that he often wakes her up. She notes that her husband sometimes appears not to take a breath for a long time and then gasps for air before continuing to snore. He suffers from daytime headaches and sleepiness. He has a body mass index (BMI) of 40 kg/m2.

What would the most likely arterial blood gas result be if it was measured in this patient?

Compensated respiratory acidosis
Compensated respiratory alkalosis
Compensated metabolic acidosis
Uncompensated respiratory acidosis
Uncompensated metabolic acidosis

A

Compensated respiratory acidosis

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10
Q

Describe what hypoglossal nerve stimulation is [1]
How does it work? [1]

A

Hypoglossal nerve stimulation aims to treat obstructive sleep apnoea by preventing the tongue prolapsing backwards and causing upper airway obstruction during sleep. It works by delivering an electrical current to the hypoglossal nerve

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11
Q

What trio of crtieria make a diagnosis of obesity hypoventilation syndrome? [3]

A
  • Daytime hypercapnia PaCO2 ≥ 45 mmHg
  • Obesity (BMI > 30)
  • Sleep disordered breathing (which can include OSA)
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12
Q

How do you determine obesity hypoventilation syndrome vs OSA? [1]

A

Daytime hypercapnia in OHS

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13
Q

What is the treatment for OHS? [1]

A

First line:
- CPAP

Second line:
- NIV

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14
Q

Desribe a key difference in OSA and OHS [1]

A

Patients with OHS often experience daytime hypoventilation, which leads to chronic hypercapnia and hypoxemia, resulting in symptoms such as dyspnea, exercise intolerance, morning headaches, and cognitive dysfunction.

In summary, OHS is a more complex disorder involving chronic hypoventilation, obesity, and sleep-disordered breathing, whereas OSA is specifically characterized by upper airway obstruction during sleep

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15
Q

Which type of hypersensitivty is asthma? [1]

A

Type 1

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16
Q

Describe the pathophysiology of asthma

A

Airway inflammation:
- Immune cells activated by TH2, mast cells and eosinophils
- Causes pro-inflam mediators (cytokines, chemokines, histamines, leukotrines) to cause airway oedema, mucus production, and bronchoconstriction

Bronchoconstriction
- narrowing of the airways and obstruction of airflow.

Airway hyperresponsiveness
- airways exhibit excessive narrowing in response to various stimuli, such as allergens, irritants, and cold air
- mediated by several factors, including the release of inflammatory mediators, increased airway smooth muscle contractility, and impaired bronchodilator mechanisms

Mucus production and airway remodeling:
* Chronic inflammation causes airway remodeling
* Subepithelial fibrosis, increased smooth muscle mass, mucus gland hypertrophy, and angiogenesis.

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17
Q

A number of patients with asthma are sensitive to which drug? [1]

Patients who are most sensitive to asthma often suffer from []? [1]

A

A number of patients with asthma are sensitive to aspirin.

Patients who are most sensitive to asthma often suffer from nasal polyps. Remember the nose is part of the respiratory tract from a histological point of view.

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18
Q

Describe the pathway that causes asthma [5]

A

i. Allergen picked up by dendritic cells and presented by MHC Class II molecules
ii. CD4 cells activate the TH-2 lymphocytes through the release of IL4, IL5, IL13.
iII. IL 4 leads to the production of IgE antibodies: coat mast cells and stimulate degranulation and the release histamines, leukotrienes and prostaglandins
iv. IL-5 activates eosinophils: causes more cytokine & leukotrienes release
v IL-9 = mast cell proliferation

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19
Q

What are the classical features of asthma? [4]

What helps to create a clinical picture regarding features and treatment? [1]

A

episodic symptoms; typically worse at night:
* widespread, polyphonic expiratory wheeze (occurs from turbulent airflow in narrow airways)
* breathlessness
* chest tightness: airway obstruction and increasde work of breathing
* cough: dry or productive; worse at night or early in morning.

Symptoms should improve with bronchodilators. No response to bronchodilators reduces the likelihood of asthma.

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20
Q

TOM TIP: A localised monophonic wheeze is not asthma.

Give the top differentials of a localised wheeze [3]

A

Inhaled foreign body
tumour
a thick sticky mucus plug obstructing an airway (pneumonia)
pulmonary oedema

A chest x-ray is the next step.

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21
Q

Which drugs can worsen asthma? [3]

A

Non-selective beta blockers: propranolol
- blocking the beta receptors in the lungs, which leads to bronchoconstriction and breathing difficulties.

Non-steroidal anti-inflammatory drugs: aspirin, ibuprofen or naproxen
- This reaction is known as aspirin-exacerbated respiratory disease (AERD) or aspirin-induced asthma.

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22
Q

Which cells are responsible for the acute phase of asthma? [1]

Which cells are responsible for the late phase of asthma? [3]

A

Early: mast cells

Late: Th2 helper cells –> B cells –> IgE & Eiosinophils

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23
Q

Describe the features that would make you suspicious that a patient has asthma [6]

A

More than one of the following in episodes:
 wheeze
 breathlessness
 chest tightness
 cough

diurnal variability

Triggered by allergen, exercise, cold air, aspirin or β-blocker

Atopic features
 Eczema
 Hayfever

Fx

Low PEFR or FEV (note: both decrease with age)

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24
Q

Describe the diagnostic pathway for diagnosis of asthma

A
  1. Clinical suspicion based off clinical assessment (history, exam, previous medical records)
  2. IF high probabilty of asthma:
     Code as suspected asthma and start treatment
    Assess response to treatment:
    Good response = asthma;
    poor response then intermediate probability of asthma.
  3. Next: Test for airway obstruction using spirometry and bronchodilator reversibility:
  • Test for variability by investigating:
     Reversibility
     PEF charting
     Challenge tests
  • Test for eosinophilic inflammation:
     FeNO
     Blood eosinophs
     Skin prick test, IgEIf good response: asthma
    If poor response: investigate other more likely diagnosis

BTS pathway

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25
Q

What does FeNO test? [1]

What level of FeNO would be considered positive for asthma in adults? [1]
What level of FeNO would warrent further consideration for asthma positive for asthma in adults? [1]
What level of FeNO would you consider a different diagnosis than asthma in adults? [1]

A

fractional exhaled nitric oxide (FeNO):

FeNO tests the amount of NO produced by iNOS, which is raised in eisinophils (which are raised in asthma)

  • in adults a level of >= 40 parts per billion (ppb) is considered positive
  • 25-39 ppb would warrant further investigations
  • < 25 ppb would be a different diagnosis
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26
Q

What level of FeNO would be considered positive for asthma in children? [1]

A
  • in children a level of >= 35 parts per billion (ppb) is considered positive
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27
Q

What would indicate positive reversibility testing in adults [2] and children [1]?

A

Reversibility testing:
- in adults, a positive test is indicated by an improvement in FEV1 of 12% or more and increase in volume of 200 ml or more
- in children, a positive test is indicated by an improvement in FEV1 of 12% or more

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28
Q

Describe what is meant by direct bronchial challenge testing [1]

What results would indicate a positive result for asthma? [1]

A

Direct bronchial challenge testing is the opposite of reversibility testing.

Inhaled histamine or methacholine is used to stimulate bronchoconstriction, reducing the FEV1 in patients with asthma.

NICE say a PC20 (provocation concentration of methacholine causing a 20% reduction in FEV1) of 8 mg/ml or less is a positive test result.

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29
Q

How long would you ask a patient to keep a peak flow diary for when investigating asthma? [1]

What results would indicate a positive result for asthma? [1]

A

Peak flow variability is measured by keeping a peak flow diary with readings at least twice daily over 2 to 4 weeks.

NICE says a peak flow variability of more than 20% is a positive test result, supporting a diagnosis.

PEF: 20%
FEV1: 12% or 200ml

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30
Q

Label A-E [5]

A

A: FEV1/FVC< 70%
B: >12% or 200ml improvement in FEV1
C: >40 ppb
D: concentration required to cause 20% fall in FEV1 (PC20) OF 8mg/ml or less
E: 20% variability

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31
Q

What do you give patients when performing bronchial provocation testing? [1]

Describe how you pefrom bronchial provocation testing [2]

A

Bronchial provocation testing is performed with methacholine or histamine

Increasing doses are given until the patient’s forced expiratory volume (FEV1) drops by 20% in one second. This dose is termed the PC20.

A PC20 dose of 8 mg/ml or less reflects a positive result.

32
Q

What do you need to tell patients (in an OSCE) about reviewing medication? [1]

A

Specialist nurses help to make changes to medication

Review post discharge (< 30 days)

33
Q

What five steps should you educate / make on self management plans for patietns? [5]

A

How to use treatment
Self monitoring/assessment skills
Action plan with regard to goals
Recognition and management of exacerbations
Allergen/trigger avoidance

34
Q

Name two drugs used for reliever medication for asthma? [1]

State the class of drug [1] and MoA [2]

A

Name:
* Salbutamol
* terbutaline

Class:
* beta 2 agonist

MoA:
- relax smooth muscle to cause bronchodilation and mucociliary clearane
- relieve bronchospasm

35
Q

Name three inhaled corticosteroids used to as long term asthma tx [3]

A

o budesonide
o beclometasone
o fluticasone

36
Q

What are the side effects of ICS treatment for asthma? [3]

A

Sore throat
Oral candidiasis
Cough

37
Q

What are low [1], moderate [1] and high doses [1] used ICS in asthma tx? [3]

A

Low dose:
* <= 400 micrograms budesonide or equivalent

Medium dose:
* 400 micrograms - 800 micrograms budesonide or equivalent

High dose:
* > 800 micrograms budesonide or equivalent

38
Q

Name a LAMA

A

tiotropium

39
Q

Name an anti-IgE medication [1]

A

Omalizumab

40
Q

Describe the MoA of Omalizumab [1]

When is it indicated? [2]

A

Mechanism of action:
* monoclonal antibody to IgE
* decreases IgE

Considered when:
* confirmed allergic IgE-mediated asthma as an add-on to optimised standard therapy after all others used
* suffer from asthma with continuous or frequent treatment with oral corticosteroids (defined as 4 or more courses in the previous year)

41
Q

Name 4 AEs of omalizumab [4]

A
  • itching
  • joint pain
  • headache
  • nausea
  • anaphylaxis
42
Q

State the treatment algorithm for asthma

A
  1. Newly-diagnosed asthma:
    SABA; (salbutamol)
  2. Inhaled corticosteroid (low dose) taken regularly
  3. BTS: Long-acting beta-2 agonists (e.g., salmeterol) or maintenance and reliever therapy (MART)
    OR
    NICE: Leukotriene receptor antagonist (e.g., montelukast) taken regularly
  4. BTS: Increase the inhaled corticosteroid or add a leukotriene receptor antagonist (e.g., montelukast)
    OR
    NICE: Long-acting beta-2 agonists (e.g., salmeterol) taken regularly
  5. BTS: Specialist management(e.g., oral corticosteroids)
    OR
    NICE: Consider changing to a maintenance and reliever therapy (MART) regime
  6. NICE: Increase the inhaled corticosteroid to a moderate dose
  7. NICE: Consider high-dose inhaled corticosteroid or additional drugs (e.g., LAMA or theophylline)
43
Q

Give three definitions of uncontrolled asthma (when you increase up the ladder) [3]

A
  • 3 or more days a week with symptoms or
  • 3 or more days a week with required use of a SABA for symptomatic relief or
  • 1 or more nights a week with awakening due to asthma.
44
Q

A 21-year-old woman attends for her annual asthma review. She reports having her usual symptoms of shortness of breath, wheeze and chest tightness around 3 times per week. These symptoms typically occur at night and she wakes up feeling wheezy around once per week. She currently only uses a salbutamol inhaler as required and gets good relief from this.

The patient otherwise has no medical history, takes no other medications and has no allergies.

How should this patient be managed?

Add a budesonide inhaler

Add a salmeterol inhaler

Add oral montelukast and a beclomethasone inhaler

Continue current salbutamol only

Switch to regular salbutamol

A

Add a budesonide inhaler

Adult with asthma not controlled by a SABA - add a low-dose ICS

45
Q

What effect do B2-agonists have on lactate levels? [1]

A

Increase lactate levels

46
Q

What is a common choice for SABA dose? [1]

A

Salbutamol 100-200 micrograms inhaled as required

47
Q

What advice should you give about reliever medication and exercise? [1]

A

Take 10 mins before excercise

48
Q

Anti-muscarinics are contraindicated in which diseases? [2]

A

Arrhythmias
Urinary retention

49
Q

What is important to note about taking ICS? [1]
How do you combat this? [1]

A

In some patients can cause paradoxical bronchospasm
Take SABA before to counteract.

50
Q

State what you information you would say when prescribing ICS to a patient [3]

A

ICS ‘dampens down’ the immune system and inflammation of the lung

Wont feel immediate benefits after inhalation, treatment should gradually improve symptoms and flare ups, if taken regularly

Common side effects include a sore throat or horse throat, which can be minimised by rinsing or gargling with water after treatment

51
Q

1/100 who take montelukast suffer from what type of symptoms? [1]

Give examples [2]

A

Neuropsychiatric reactions: sleep disturbance, depression, agitation

52
Q

Describe the technique you should give patients with regards to inhaler technique.

A

If haven’t used it in 5 days or more / new - need to test: take cap off and shake well, undergo test spray

check that the inhaler dose counter is not at 0

check that there is nothing inhaler mouth piece

shake inhaler

sit / stand up straight and tilt head up

gently and slowly breath out away from inhaler

put lips around inhaler and form tight seal

slow and steady breath in and press inhaler once

continue breathing until lungs feel full

take inhaler off mouth and hold breath for 10 secs / as long as poss

breath out gently

if prescribed a second puff, wait 30 secs and repeat

if used steroids: wash mouth out

53
Q

What is the rule about caring for pregnant asthma patients? [1]

A

Pregnant women who have a severe asthma attack should be admitted to hospital, EVEN if they initially improve with treatment

54
Q

Terbutaline is which of the following drug class

SAMA
SABA
LAMA
LABA

A

Terbutaline is which of the following drug class

SAMA
SABA
LAMA
LABA

55
Q

Tiotropium is which of the following drug class

SAMA
SABA
LAMA
LABA

A

Tiotropium is which of the following drug class

SAMA
SABA
LAMA
LABA

56
Q

How does omalizumab work to treat asthma? [1]

A

It works by inhibiting binding of IgE to its receptor, located on mast cells and basophils. This action prevents release of mediators of allergic response (e.g., histamine) that cause bronchospasm.

57
Q

Which of the following drug class, if prescribed without ICS, can increase chance of death in asthma patients?

SAMA
SABA
LAMA
LABA

A

Which of the following drug class, if prescribed without ICS, can increase chance of death in asthma patients?

SAMA
SABA
LAMA
LABA

58
Q

What does recruitment mean? [1]

A

Recruitment refers to a process where bronchioles and alveoli which would normally collapse at the end of expiration, are kept open (more lung volume is ‘recruited’).

The phase of breathing that requires the most energy is the process of overcoming the pressure required to re-expand collapsed segments of the lung

59
Q

When [5] and where [2] is NIV indicated?

A

Acute T2RF: COPD exacerbations
- Inpatient

Chronic T2RF: At home
- Kyphoscoliosis
- Neuromuscular
- Obesity hypoventilation syndrome
- COPD

60
Q

Which complications of hypoxia does long term oxygen therapy reduce? [2]

A

Cor pulmonale
Polycythaemia

61
Q

Describe how NIV works to provide O2 therapy [3]

A

NIV delivers differing air pressure depending on inspiration and expiration.

The inspiratory positive airways pressure (iPAP) is higher than the expiratory positive airways pressure (ePAP).

Therefore, ventilation is provided mainly by iPAP, whereas ePAP recruits underventilated or collapsed alveoli for gas exchange and allows for the removal of the exhaled gas.

62
Q

Explain how CPAP works (when providing oxygen therapy) [1]

A

CPAP supplies constant fixed positive pressure throughout inspiration AND expiration. It, therefore, is not a form of ventilation, but splints the airways open

63
Q

What are the indications for CPAP? [4]

A
  • Hypoxia in the context of chest wall trauma despite adequate anaesthesia and high flow oxygen (pneumothorax should be ruled out using a chest x-ray prior to commencing CPAP)
  • Cardiogenic pulmonary oedema
  • Pneumonia: as an interim measure before invasive ventilation or as a ceiling of treatment
  • Obstructive sleep apnoea
64
Q

CPAP is often started at [] H2O and gradually increased to reduce hypoxia.

NIV is often started at iPAP [] and ePAP []

H2O is typically increased in [] cm intervals by approximately [] cms every [] minutes until a therapeutic response is achieved.

A

CPAP is often started at 4cm H2O and gradually increased to reduce hypoxia.

NIV is often started at iPAP 10 and ePAP 4.4

H2O is typically increased in 2-5cm intervals by approximately 5cms every 10 minutes until a therapeutic response is achieved.

65
Q

Based on current evidence CPAP & NIV pressures should not exceed [] cm H2O at any point.

A

Based on current evidence CPAP & NIV pressures should not exceed 25 cm H2O at any point.

66
Q

What are the different colours of venturi mask colours? [6]

What are the oxygen flow rate (L/min) for these different colours of venturi mask? [6]

What are the FiO2 (approx. oxygen) delivered for these different colours of venturi mask? [6]

A
67
Q

Label A-F

A

A: Blue
B: White
C: Orange
D: Yellow
E: Red
F: Green

68
Q

Label A-F

A

A: 24%
B: 28%
C: 31%
D: 35%
E: 40%
F: 60%

69
Q

How does a high-flow nasal cannula work? [3]

A

Reduces the amount of room air that the patient inhales alongside the supplementary oxygen, increasing the concentration of oxygen inhaled with each breath.

It also adds some positive end-expiratory pressure to help prevent the airways from collapsing at the end of exhalation (although this effect is reduced if the patient opens their mouth).

Also, provides dead space washout: normally, dead space is ar that remains in airwaays and oropharnyx, not undergoing respiration. High-flow oxygen effectively clears this and replaces it with oxygen, improving patient oxygenation.

70
Q

What are some key modes of MV? [4]

A

Volume controlled ventilation (VC) – the machine is set to deliver a specific tidal volume per breath

Pressure controlled ventilation (PC) – the machine is set to deliver a specific pressure per breath

Assist control (AC) – breaths are triggered by the patient (or by the machine if there is no respiratory effort)

Continuous positive airway pressure (CPAP) – the patient breathes while the machine adds constant pressure

71
Q

Explain what is meant by Acute Respiratory Distress Syndrome [2]

ARDS has an acute onset of which pathological features? [4]

A

ARDS: Severe inflammatory reaction in the lungs, often secondary to sepsis or trauma.

Only a small portion of the total lung volume is aerated and has functional alveoli. The remainder of the lungs are collapsed and non-aerated.

There is an acute onset of:
* Collapse of the alveoli and lung tissue (atelectasis)
* Pulmonary oedema (not related to heart failure or fluid overload)
* Decreased lung compliance (how much the lungs inflate when ventilated with a given pressure)
* Fibrosis of the lung tissue (typically after 10 days or more)

72
Q

Describe the clinical presentation of ARDS [4]

A
  • Acute respiratory distress
  • Hypoxia (with an inadequate response to oxygen therapy)
  • elevated respiratory rate
  • bilateral lung crackles
  • pO2/FiO2 < 40kPa (200 mmHg)
73
Q

What is the management of ARDS? [5]

A
  • Due to the severity of the condition patients are generally managed in ITU:
  • Respiratory support to treat hypoxaemia
  • Prone positioning (lying on their front)
  • Careful fluid management to avoid excess fluid collecting in the lung
  • General organ support e.g. vasopressors as needed
  • Treatment of the underlying cause e.g. antibiotics for sepsis
74
Q

Explain what is meant by central sleep apnea (CSA). What are the two mechanisms involved with CSA? [2]

A

Central sleep apnea (CSA) is caused by alterations in respiratory drive, which during sleep is highly dependent on carbon dioxide levels. Two mechanisms are distinguished:

Hypoventilation-related CSA:
- Decreased ventilatory drive causes transient decreases and/or pauses in respiration.

Hyperventilation-related CSA:
- Increased ventilatory drive during sleep leads to hypocapnia which causes a compensatory fall in ventilation that, if abnormally prolonged, leads to recurrent central apnea with arousals.

75
Q

Name some causes of central sleep apnea (both hypoventilation related and hyperventilation) [5]

A

Causes of hypoventilation-related CSA with hypercapnia
- hypothyroidism
- neural lesions (eg, brain stem infarctions, encephalitis, Chiari II type malformation)
- certain drugs (most commonly opioids—including methadone).

Hyperventilation-related CSA:
- occurs at high altitude in healthy people as a consequence of hypobaric hypoxia.
- It also occurs in patients with heart failure and occasionally during treatment of obstructive apneas.

76
Q
A